Commensal and Pathogenic Escherichia coli Metabolism in the Gut
- Authors: Tyrrell Conway1, Paul S. Cohen2
- Editors: Tyrrell Conway3, Paul Cohen4
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VIEW AFFILIATIONS HIDE AFFILIATIONSAffiliations: 1: Department of Microbiology and Molecular Genetics, Oklahoma State University, Stillwater, OK 74078; 2: Department of Cell and Molecular Biology, University of Rhode Island, Kingston, RI; 3: Oklahoma State University, Stillwater, OK; 4: University of Rhode Island, Kingston, RI
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Received 25 July 2014 Accepted 29 July 2014 Published 25 June 2015
- Correspondence: Tyrrell Conway, [email protected]

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Abstract:
E. coli is a ubiquitous member of the intestinal microbiome. This organism resides in a biofilm comprised of a complex microbial community within the mucus layer where it must compete for the limiting nutrients that it needs to grow fast enough to stably colonize. In this article we discuss the nutritional basis of intestinal colonization. Beginning with basic ecological principles we describe what is known about the metabolism that makes E. coli such a remarkably successful member of the intestinal microbiota. To obtain the simple sugars and amino acids that it requires, E. coli depends on degradation of complex glycoproteins by strict anaerobes. Despite having essentially the same core genome and hence the same metabolism when grown in the laboratory, different E. coli strains display considerable catabolic diversity when colonized in mice. To explain why some E. coli mutants do not grow as well on mucus in vitro as their wild type parents yet are better colonizers, we postulate that each one resides in a distinct “Restaurant” where it is served different nutrients because it interacts physically and metabolically with different species of anaerobes. Since enteric pathogens that fail to compete successfully for nutrients cannot colonize, a basic understanding of the nutritional basis of intestinal colonization will inform efforts to develop prebiotics and probiotics to combat infection.
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Citation: Conway T, Cohen P. 2015. Commensal and Pathogenic Escherichia coli Metabolism in the Gut. Microbiol Spectrum 3(3):MBP-0006-2014. doi:10.1128/microbiolspec.MBP-0006-2014.




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Abstract:
E. coli is a ubiquitous member of the intestinal microbiome. This organism resides in a biofilm comprised of a complex microbial community within the mucus layer where it must compete for the limiting nutrients that it needs to grow fast enough to stably colonize. In this article we discuss the nutritional basis of intestinal colonization. Beginning with basic ecological principles we describe what is known about the metabolism that makes E. coli such a remarkably successful member of the intestinal microbiota. To obtain the simple sugars and amino acids that it requires, E. coli depends on degradation of complex glycoproteins by strict anaerobes. Despite having essentially the same core genome and hence the same metabolism when grown in the laboratory, different E. coli strains display considerable catabolic diversity when colonized in mice. To explain why some E. coli mutants do not grow as well on mucus in vitro as their wild type parents yet are better colonizers, we postulate that each one resides in a distinct “Restaurant” where it is served different nutrients because it interacts physically and metabolically with different species of anaerobes. Since enteric pathogens that fail to compete successfully for nutrients cannot colonize, a basic understanding of the nutritional basis of intestinal colonization will inform efforts to develop prebiotics and probiotics to combat infection.

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Figures

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FIGURE 1
Nutrient flow in the intestine. The primary sources of carbohydrates in the large intestine are mucus, dietary fiber, and epithelial cell debris. Mucus and dietary fiber consist of complex polysaccharides. E. coli typically cannot degrade complex polysaccharides; that is the job of anaerobes. Hence, degradation of polysaccharides by anaerobes releases oligosaccharides, which are preferred by anaerobes, as well as mono- and disaccharides, which are preferred by E. coli.
Tables

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TABLE 1
Central metabolism mutants tested for colonization defects in the mouse intestine

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TABLE 2
Sugar utilization in the intestine by E. coli strains
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